Spermatogenesis and its endocrine regulation
Spermatogenesis and its endocrine regulation
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DOI：
10.1023/a:1023303427191
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发表时间：
2004
影响因子：
2.9
通讯作者：
R. Schulz;T. Miura
中科院分区：
文献类型：
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作者：
R. Schulz;T. Miura
精子发生有三个主要阶段：精原细胞有丝分裂、精母细胞减数分裂和精子发生，即精子细胞重组为有鞭毛的精子。这一过程由干细胞推动，干细胞在分裂时要么自我更新，要么产生精原细胞，这些精原细胞致力于增殖、减数分裂和精子形成。在所有阶段，生殖细胞都与支持细胞密切接触，并需要支持细胞的结构和功能支持。与生殖细胞不同，这些体细胞表达性类固醇和卵泡刺激素(FSH)的受体，这是调节精子发生的最重要的激素。Sertoli细胞对内分泌刺激的典型反应是改变一种生长因子的释放，然后该生长因子将介导激素对生殖细胞的影响。例如，最近对日本鳗鱼的研究表明，在缺乏促性腺激素的情况下，Sertoli细胞会产生一种生长因子(抗缪勒激素的同源产物)，将干细胞分裂限制在自我更新途径上；雌激素也会刺激干细胞更新分裂，但不会刺激精原细胞的增殖。然而，促性腺激素或11-酮睾酮(11-KT)刺激可诱导精原细胞增殖，这在一定程度上被另一种支持细胞衍生生长因子(激活素B)所模仿。由于FSH(除促黄体激素外)刺激鱼类的类固醇生成，而且FSH是在性未成熟鲑鱼血浆中检测到的唯一促性腺激素，增加FSH信号可能足以通过激活Sertoli细胞功能和11-KT产生来启动精子发生。另一种重要的雄激素是睾酮(T)，它似乎通过反馈机制发挥作用，这种反馈机制可以损害FSH依赖的信号或类固醇的生成。因此，睾丸T和11-KT的产生需要充分平衡。需要进一步的研究来阐明(S)11-KT如何刺激发育的后期阶段，如进入减数分裂和精子发生。在这个时期，黄体生成素对调节雄激素的产生变得越来越重要。哺乳动物模型的结果表明，在晚期，通过支持细胞因子控制生殖细胞凋亡是一种重要的调控机制。在许多物种中，精子细胞只有在经历了被称为获能的成熟过程后才能使卵子受精，这一成熟过程包括获得运动能力。在黄体生成素的影响下产生的孕激素似乎在这方面发挥了重要作用，这涉及到控制精浆的成分(例如，pH值)。
Three major phases compose spermatogenesis: mitotic proliferation of spermatogonia, meiosis of spermatocytes, and spermiogenesis, the restructuring of spermatids into flagellated spermatozoa. The process is fuelled by stem cells that, when dividing, either self-renew or produce spermatogonia that are committed to proliferation, meiosis, and spermiogenesis. During all phases, germ cells are in close contact with and require the structural and functional support of Sertoli cells. In contrast to germ cells, these somatic cells express receptors for sex steroids and follicle-stimulating hormone (FSH), the most important hormones that regulate spermatogenesis. A typical Sertoli cell response to an endocrine stimulus would be to change the release of a growth factor that would then mediate the hormone's effect to the germ cells. Recent studies in the Japanese eel have shown, for example, that in the absence of gonadotropin Sertoli cells produce a growth factor (an orthologue of anti-Müllerian hormone) that restricts stem cell divisions to the self-renewal pathway; also estrogens stimulate stem cell renewal divisions but not spermatogonial proliferation. Gonadotropin or 11-ketotestosterone (11-KT) stimulation, however, induces spermatogonial proliferation, which is in part mimicked by another Sertoli cell-derived growth factor (activin B). Since FSH (besides luteinizing hormone, LH) stimulates steroidogenesis in fish, and since FSH is the only gonadotropin detected in the plasma of sexually immature salmonids, increased FSH signalling may be sufficient to initiate spermatogenesis by activating both Sertoli cell functions and 11-KT production. Another important androgen is testosterone (T), which seems to act via feedback mechanisms that can compromise FSH-dependent signalling or steroidogenesis. The testicular production of T and 11-KT therefore needs to be balanced adequately. Further research is required to elucidate in what way(s) 11-KT stimulates later stages of development, such as entry into meiosis and spermiogenesis. At this period, LH becomes increasingly important for the regulation of androgen production. Results from mammalian models suggest that during the later phases, the control of germ cell apoptosis via Sertoli cell factors is an important regulatory mechanism. In many species, sperm cells cannot fertilize eggs until having passed a maturation process known as capacitation, which includes the acquisition of motility. Progestins that are produced under the influence of LH appear to play an important role in this context, which involves the control of the composition of the seminal plasma (e.g., pH values).